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Objective To investigate the therapeutic effect of Enalapril Maleate and Folic Acid Tablets in the treatment of type H hypertension complicated with coronary heart disease.MethodsA total of 80 patients with type H hypertension complicated with coronary heart disease admitted in our hospital from January 2014 to January 2016 were selected.They were randomly divided into control group and observation group.The control group was treated with enalapril maleate, while the observation group was treated with Enalapril Maleate and Folic Acid Tablets.The total effective rate of two groups of patients were analyzed and compared.ResultsAfter 6 months of treatment, the total effective rate of the observation group was significantly higher than that of the control group, the total effective rate of the observation group was 95.00%, and the total effective rate of the control group was 77.50%(P<0.05), the difference was statistically significant.ConclusionThe effect of Enalapril Maleate and Folic Acid Tablets in the treatment of type H hypertension complicated with coronary heart disease is obvious, and it can improve the total effective rate of the treatment.
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Aim To investigate the effect of salvianolic acid B (Sal B)on c-Jun N-terminal kinase (JNK)ac-tivation and apoptosis of INS-1 cells induced by inter-mittent high glucose.Methods INS-1 cells were pre-incubated with Sal B for 24 h,followed by exposure to intermittent high glucose (IHG,11.1 mmol·L-1 12 h,33. 3 mmol·L-1 12 h)for 72 h.Cell viability was assessed by MTT assay and cell apoptosis was evalua-ted by flow cytometry.Glucose induced insulin secre-tion capacity and intracellular reactive oxygen species (ROS)contents were measured by enzyme linked im-munosorbent assay (ELISA)and a fluorescent probe DCFH-DA,respectively.Levels of JNK activation and PDX-1 protein expression were determined by Western blot analysis.Results Sal B significantly alleviated IHG-induced cell injury and apoptosis,with glucose induced insulin secretion capacity improved evidently (P<0.05 or P<0.01).Preincubation with Sal B no-tably decreased intracellular ROS and JNK activation in INS-1 cells,while the level of PDX-1 protein was in-creased markedly (P<0.05 or P<0.01 ).Conclu-sion Sal B is capable of ameliorating IHG-induced cell injury and apoptosis in INS-1 cells,which might be derived from suppression of JNK activation and up-regulation of PDX-1 protein expression.
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Objective To investigate the effect of astragalus injection combined with beta-adrenoceptor antagonist on serum levels of brain natriuretic peptide ( BNP) , interleukin1β( IL-1β) , IL-6 and tumor necrosis factorα( TNF-α) in the treatment of elderly patients with heart failure. Methods 78 elderly patients with heart failure from April 2013 to April 2015 in department of cardiology of the second hospital of Yuhang district were selected and divided into control group and experimental group with 39 cases in each group.All patients received correction of the electrolyte and acid-base balance and other conventional treatment.The control group received carvedilol by oral, the experimental group received astragalus injection on the basis of control group, with a course of 30 days.The serum BNP,IL-1β,IL-6 and TNF-αlevels pre-and post-treatment in two groups were compared. Results Compared with pre-treatment, the serum IL-1β,IL-6,TNF-α,and BNP levels post-treatment in two groups were lower(P<0.05).Compared with the control group post-treatment, the IL-1β,IL-6,TNF-αand BNP levels in experimental group were lower(P <0.05).Conclusion Astragalus injection combined with beta-adrenoceptor antagonist could significantly improve the clinical sign of elderly patients with heart failure, the mechanism may be reducing the serum levels of IL-1β,IL-6,TNF-αand BNP.
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AIM:To study the effects of sesamin (Ses) on attenuating renal injury in spontaneously hyperten-sive rats (SHR) and its relationship with PI3K/AKT/mTOR signaling pathway.METHODS:Spontaneously hypertensive rats were randomly divided into 4 groups:model (SHR) group, Ses low-dose (80 mg/kg) group, Ses high-dose (160 mg/kg) group and captopril (30 mg/kg) group.Another 7 WKY rats were given 0.5%sodium carboxymethylcellulose ( CMC-Na, the solvent was used to dissolve the drugs) as control group.Meanwhile, the rats in drug treatment groups were given the corresponding drugs.All animals were administered intragastrically once a day, and the blood pressure was measured every 2 weeks before and after the beginning of the administration.After 12 weeks, blood urea nitrogen ( BUN) , serum creatinine ( SCr ) , urine micro-albumin ( U-mAlb ) , malondialdehyde ( MDA ) and superoxide dismutase ( SOD ) were measured.The pathological changes of the renal tissues were observed under microscope with HE and Masson staining.Ap-optotic rate of nephridial tissue was determined by TUNEL method.The protein levels of p-AKT, p-mTOR, 4EBP1, S6K1, Bcl-2 and Bax were detected by Western blot.RESULTS:Ses decreased the diastolic blood pressure of SHR, significantly ameliorated the pathological damage in the nephridial tissues.Compared with model group, Ses was obviously reduced the contents of SCr, BUN, U-mAlb, MDA and apoptotic rate of the kidney, decreased the protein levels of p-AKT, p-mTOR, 4EBP1, S6K1 and Bax, and increased the protein expression of Bcl-2 and SOD activity.CONCLUSION:The protective effects of Ses against renal injury in SHR may be related to decreasing blood pressure, increasing anti-oxidative stress, re-straining apoptosis and inhibiting over-activated PI3K/AKT/mTOR signaling pathway.
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Crocetin, a naturally occurring carotenoid, possesses antioxidant and antiatherosclerotic properties, of which the underlying mechanism remains unclear. In the present study, we examined the effects of crocetin (0.1, 1, 10 μmol·L(-1)) on angiotensin II (Ang II, 0.1 μmol·L(-1)) induced expression of vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) and monocyte-endothelial cell adhesion. The effects of crocetin on the activation of nuclear factor kappa B (NF-κB) and intracellular reactive oxygen species (ROS) were also observed. The results demonstrated that crocetin notably suppressed Ang II induced NF-κB activation (P<0.01) and VCAM-1 expression (P<0.05, P<0.01) in HUVECs, accompanied by a markedly reduced monocyte-endothelial cell adhesion (P<0.05, P<0.01). In addition, preincubation with crocetin resulted in a significant enhancement of cellular antioxidant capacity (P<0.05, P<0.01), while Ang II induced intracellular ROS decreased markedly (P<0.05, P<0.01). These results indicated that crocetin was capable of suppressing Ang II induced VCAM-1 expression and monocyte-endothelial cell adhesion by suppression of NF-κB activation, which might be derived from the enhancement of antioxidant capacity and subsequent reduction of intracellular ROS.